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@ARTICLE{Wischhof:272912,
author = {Wischhof, Lena and John Mathew, Amal and Bonaguro, Lorenzo
and Beyer, Marc and Ehninger, Dan and Nicotera, Pierluigi
and Bano, Daniele},
title = {{M}itochondrial complex {I} inhibition enhances astrocyte
responsiveness to pro-inflammatory stimuli},
journal = {Scientific reports},
volume = {14},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {DZNE-2024-01317},
pages = {27182},
year = {2024},
abstract = {Inhibition of the mitochondrial oxidative phosphorylation
(OXPHOS) system can lead to metabolic disorders and
neurodegenerative diseases. In primary mitochondrial
disorders, reactive astrocytes often accompany neuronal
degeneration and may contribute to neurotoxic inflammatory
cascades that elicit brain lesions. The influence of
mitochondria to astrocyte reactivity as well as the
underlying molecular mechanisms remain elusive. Here we
report that mitochondrial Complex I dysfunction promotes
neural progenitor cell differentiation into astrocytes that
are more responsive to neuroinflammatory stimuli. We show
that the SWItch/Sucrose Non-Fermentable (SWI/SNF/BAF)
chromatin remodeling complex takes part in the epigenetic
regulation of astrocyte responsiveness, since its
pharmacological inhibition abrogates the expression of
inflammatory genes. Furthermore, we demonstrate that Complex
I deficient human iPSC-derived astrocytes negatively
influence neuronal physiology upon cytokine stimulation.
Together, our data describe the SWI/SNF/BAF complex as a
sensor of altered mitochondrial OXPHOS and a downstream
epigenetic regulator of astrocyte-mediated
neuroinflammation.},
keywords = {Astrocytes: metabolism / Astrocytes: drug effects / Humans
/ Electron Transport Complex I: metabolism / Electron
Transport Complex I: genetics / Electron Transport Complex
I: antagonists $\&$ inhibitors / Mitochondria: metabolism /
Oxidative Phosphorylation: drug effects / Induced
Pluripotent Stem Cells: metabolism / Induced Pluripotent
Stem Cells: cytology / Cell Differentiation / Epigenesis,
Genetic / Neural Stem Cells: metabolism / Neural Stem Cells:
drug effects / Inflammation: metabolism / Inflammation:
pathology / Cells, Cultured / Animals},
cin = {AG Bano / AG Beyer / PRECISE / AG Ehninger / AG Schultze},
ddc = {600},
cid = {I:(DE-2719)1013003 / I:(DE-2719)1013035 /
I:(DE-2719)1013031 / I:(DE-2719)1013005 /
I:(DE-2719)1013038},
pnm = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
(POF4-352) / 354 - Disease Prevention and Healthy Aging
(POF4-354)},
pid = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
G:(DE-HGF)POF4-354},
experiment = {EXP:(DE-2719)PRECISE-20190321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39516523},
pmc = {pmc:PMC11549212},
doi = {10.1038/s41598-024-78434-y},
url = {https://pub.dzne.de/record/272912},
}